Luteolin reversed anxiety and depressive-like behavior via modulation of the NF-κB/NLRP3 inflammasome axis in the hippocampus of rats subjected to sleep deprivation.

Objectives: In this study, we assessed the impact of luteolin (LUT) on mood disorders (specifically anxiety and depression) induced by sleep deprivation (SD) by regulating pathways associated with neuroinflammation. Materials and Methods: Rapid eye movement (REM) SD was employed to induce anxiety and depression in the animal subjects. The animals were treated with PAX (15 mg/kg, positive control) and LUT (10 and 20 mg/kg) for a duration of 21 days. The anxiety and depressive disorders were evaluated using behavioral tests. Following the sacrifice of the animals, hippocampal tissues were stored for molecular investigations. Results: SD resulted in anxiety, as evidenced by the elevated plus maze test and open field test. Furthermore, the findings from the sucrose performance test, forced swimming test, and tail suspension test confirmed the presence of depressive-like behaviors in the animals. The nuclear factor kappa B (NF-κB) and NLR family pyrin domain containing 3 (NLRP3) inflammasome components, including apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC), NLRP3, and active Caspase-1, were up-regulated in the hippocampus (HC) of the animals subjected to REM SD. However, treatment with LUT demonstrated a significant reversal of the behavioral changes by modulating the NF-κB and NLRP3 inflammasome components in the HC. Conclusion: It can be concluded that LUT demonstrated antidepressant effects via regulation of the NF-κB/NLRP3 inflammasome axis components in the HC.

Periodontal Disease and Age-Related Macular Degeneration: A Meta-Analysis of 112,240 Participants.

OBJECTIVE: Epidemiological studies have shown a correlation between periodontal disease (PD) and age-related macular degeneration (AMD). However, the results have been inconsistent, and no relevant meta-analysis has been performed on this topic. Hence, we performed a meta-analysis to evaluate whether the two diseases are related. Material and Methods. The PubMed, Embase, Cochrane Library, and Web of Science databases were searched up to April 20, 2020, for related articles. Two authors independently conducted literature screening and data extraction and then used the Stata 15.1 software to calculate the relative risk (RRs) and 95% confidence intervals (CIs) to assess the association between PD and AMD. RESULTS: A total of 5 observational studies involving 112,240 participants and 5,005 AMD patients were included. The results of meta-analysis using the random-effects model showed that the incidence of AMD in PD patients was 1.35 times that of non-PD patients; the difference was statistically significant (RR = 1.35, 95%CI = 1.07-1.70, P = 0.011). Sensitivity analysis showed that the results were stable. CONCLUSIONS: PD patients have a higher risk of AMD, but the causal relationship between PD and AMD has not been confirmed. Further research should be carried out to verify the exact relationship between the two.

Different aberrant expression pattern of immune checkpoint receptors in patients with PTCL and NK/T-CL.

AIM: To better understand the T-cell immunodeficiency status in patients with peripheral T-cell lymphomas (PTCLs) and NK/T-cell lymphomas (NK/T-CLs), the T-cell inhibitory receptors expression pattern was investigated. METHODS: The expression levels of programmed death 1 (PD-1), cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), B/T lymphocyte attenuator (BTLA), lymphocyte-activation gene 3 (LAG-3), T-cell immunoglobulin-3 (TIM-3), T-cell immunoglobulin and ITIM domain (TIGIT) genes were detected in peripheral blood mononuclear cells (PBMCs) from patients and healthy volunteers by quantitative real-time-PCR, the correlation between different gene expression levels was analyzed. RESULTS: Significantly higher expression of PD-1, CTLA-4, BTLA, LAG-3, TIM-3 and TIGIT can be observed as a common characteristic in patients with PTCL or NK/T-CL. However, the coexpression pattern seemed different between subtypes. Their overexpression is also related to disease progression stage. CONCLUSION: We first characterized the expression pattern of six T-cell inhibitory receptor genes in PTCL and NK/T-CL, which might work as immune biomarkers for evaluation the immunosuppression status and help to establish the precision targets of immunotherapy.

High-dose dexamethasone induced LPS-stimulated rat alveolar macrophages apoptosis.

Prolonged administration of an excessive dose of corticosteroids proved to be harmful for patients with acute lung injury (ALI). A previous study has found that repeated administration of an excessive dose of methylprednisolone reduced alveolar macrophages (AMs) in bronchoalveolar lavage fluid (BALF) with an unknown mechanism. This study aimed to investigate the effect of excessive use of dexamethasone (Dex) on BALF AMs in vitro. Transmission electron microscopy and DNA fragmentation analysis demonstrated that 10-4 and 10-5 M Dex induced lipopolysaccharide-stimulated rat AMs apoptosis with downregulation of tumor necrosis factor-α, interleukin (IL)-12 and upregulation of IL-10, transforming growth factor-ß. These results indicated that apoptosis might be a novel contribution involved in the detrimental effect of excessive dose of Dex clinically used to treat ALI.

Effect of protein kinase C on T lymphocyte proliferation and apoptosis in acute idiopathic thrombocytopenic purpura.

Previous studies have shown that T lymphocyte proliferation and apoptosis are abnormal in idiopathic thrombocytopenic purpura (ITP) children; however, the underlying regulated mechanisms in signal transductions remain unknown. In this paper, we investigated the changes of protein kinase C (PKC) activity in peripheral blood T lymphocytes and the effect of PKC on the peripheral blood T lymphocyte proliferation and apoptosis in ITP children. We demonstrated that T lymphocytes from ITP children were more susceptible to the activator (phorbol myristate acetate) and the inhibitor (H-7) of PKC. In ITP children, phorbol myristate acetate and H-7 dramatically affected T lymphocyte proliferation and apoptosis, but altered little in healthy children. Compared with healthy children, PKC activity was significantly enhanced in ITP children, increasing the expressions of Fas ligand on CD3+, CD4+ and CD8+ T cells, indicating positive correlations between PKC activity and the expressions of Fas ligand on T cells, while the relations between PKC activity and platelet count showed negative correlations. Taken together, our findings suggest that PKC signal transductions may participate in the procedure of T lymphocyte proliferation and apoptosis in ITP children. PKC activation may enhance T lymphocyte activity, suppress T cell apoptosis, and be involved in thrombocyte damage, which can be related to the immunity pathogenesis of ITP.